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Neuromodulatory Control of Localized Dendritic Spiking in Critical Period Cortex

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Neuromodulatory Control of Localized Dendritic Spiking in Critical Period Cortex HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Nature. Manuscript Author Author manuscript; Manuscript Author available in PMC 2019 August 20. Published in final edited form as: Nature. 2019 March ; 567(7746): 100–104. doi:10.1038/s41586-019-0963-3. Neuromodulatory control of localized dendritic spiking in critical period cortex Courtney E. Yaeger1, Dario L. Ringach1,2, and Joshua T. Trachtenberg1 1.Department of Neurobiology, David Geffen School of Medicine at UCLA, Los Angeles, CA USA 2.Department of Psychology, University of California, Los Angeles, CA USA Abstract Sensory experience in early postnatal life, during so-called critical periods, restructures neural circuitry to enhance information processing. It is unclear why the cortex is susceptible to sensory instruction in early life and why this susceptibility wanes with age. Here, we define a developmentally-restricted engagement of inhibitory circuitry that shapes localized dendritic activity and is needed for vision to drive the emergence of binocular visual responses in mouse primary visual cortex. We find that at the peak of the critical period for binocular plasticity, acetylcholine released from the basal forebrain during periods of heightened arousal directly excites somatostatin-expressing (SST) interneurons. Their inhibition of pyramidal cell dendrites and of fast-spiking, parvalbumin-expressing (PV) interneurons enhances branch-specific dendritic responses and somatic spike rates within pyramidal cells. By adulthood, this cholinergic sensitivity is lost, and compartmentalized dendritic responses are absent but can be re-instated by optogenetic activation of SST cells. Conversely, suppressing SST cell activity during the critical period prevents the normal development of binocular receptive fields by impairing the maturation of ipsilateral eye inputs. This transient cholinergic modulation of SST cells, therefore, appears to orchestrate two features of neural plasticity – somatic disinhibition and compartmentalized dendritic spiking. Loss of this modulation may contribute to critical period closure. A major and unanswered question is what distinguishes the engagement of plasticity during critical periods of early postnatal development from that in adult cortex. In adult cortex, the necessary components of plasticity include attention and/or reinforcement1, disinhibition of pyramidal cell bodies2,3, and various forms of dendritic potentiation, including localized dendritic spiking4,5,6. Less is understood about the engagement of plasticity in the Reprints and permissions information is available at www.nature.com/reprints.Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http:// www.nature.com/authors/editorial_policies/license.html#terms Correspondence and requests for materials should be addressed to [email protected]. Author Contribution: C.E.Y., D.L.R., and J.T.T. conceived of the experiments and performed data analysis. C.E.Y. carried out all of the experiments and all of the statistical analyses. D.L.R. wrote all of the software for 2-photon acquisition, image alignment, cell identification, and temporal deconvolution. D.L.R. and J.T.T. provided oversight of the project. C.E.Y. and J.T.T. wrote the paper and prepared the figures. Competing Interests: J.T.T. is a co-owner of Neurolabware LLC. DATA AVAILABILITY The data sets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request. Yaeger et al. Page 2 developing cortex, where sensory experience exerts an extremely robust and permanent Author ManuscriptAuthor Manuscript Author Manuscript Author Manuscript Author influence on cortical circuitry. Neuromodulation and inhibition are key players in this plasticity7,8,9, but their joint influence on dendritic integration and somatic firing in pyramidal cells is not known. Dendritic compartmentalization is particularly relevant to the establishment of binocular receptive fields in primary visual cortex, which depends on a strengthening of initially weak, subthreshold ipsilateral eye input10,11 and the matching of their receptive field tuning properties to the contralateral eye12. Local dendritic spiking would enhance this process, driving the functional clustering of synaptic inputs13,14 as well as the potentiation of weak, but coactive inputs15–17. To obtain a more informed understanding of how vision drives plasticity during critical periods and why this influence is lost with age, we investigated the modulation of pyramidal neurons and the three major types of inhibitory neurons in primary visual cortex: dendrite-targeting SST cells, soma- targeting PV cells, and cells expressing the vasoactive intestinal peptide (VIP)18. We gauged cell type-specific changes in activity as a function of neuromodulation by imaging spontaneous and visually-evoked changes in fluorescence of the genetically-encoded calcium indicator GCaMP6 via resonant scanning 2-photon microscopy. These measures were made in alert, head-fixed mice running or resting on a spherical treadmill. Measurements were taken at two developmental ages – 4 weeks of age (postnatal day 28; P28) and 8 weeks of age (postnatal day 56; P56). P28 is the age of greatest sensitivity to the instructive influence of vision, and P56 is well beyond critical period closure19, in addition to being a commonly used age of study for adult mice. At P28, the spontaneous activities of SST cells increased during periods of locomotion, but by P56 this positive correlation was significantly reduced (Fig. 1a–b). Visually-evoked responses of SST cells followed a similar trend. At P28, the median change in visually- evoked GCaMP6s fluorescence was larger during locomotion than during rest, and by P56 this state-dependence was absent (Fig. 1c–d, Extended Data Fig. 1). These measures suggest that there is an age-dependent loss in the sensitivity of SST cells to neuromodulators released into cortex during running, because the reticular activating system is engaged during locomotion20,21. We tested this hypothesis in acute cortical slices by measuring evoked firing rates of SST cells in layer 2/3 of primary visual cortex to the cholinergic agonist carbachol. Supporting earlier work22–24, we found that P28 SST cells responded robustly to carbachol (2mM, bath application) when synaptic signaling of local excitatory and inhibitory neurons was blocked. Notably, this direct cholinergic response was not present at P56, despite unchanged intrinsic properties (Fig. 1e–f, Extended Data Fig. 2). Expanding on these results in vivo, we found that optogenetic stimulation of cholinergic cells in the basal forebrain drove time-locked GCaMP6s responses in SST-cells in visual cortex of P28, but not P56 mice (Fig. 1g–j). Collectively, these measures indicate that at the peak of the critical period – and not in adulthood – SST cell responses are enhanced by acetylcholine released from basal forebrain cortical projections. Because SST cells primarily receive inhibition from VIP cells18,25,26, we also measured VIP interneuron activity at both developmental time points. No age-dependent changes in the influence of behavioral state or sensitivity to carbachol were observed on VIP cell responses (Extended Data Fig. 3), consistent with prior findings22,24,27. Presumptive VIP input to SST cells also appeared to be constant with age: in acute slices of binocular vision cortex, Nature. Author manuscript; available in PMC 2019 August 20. Yaeger et al. Page 3 carbachol-mediated inhibitory currents were evident in SST cells at both ages with similar Author ManuscriptAuthor Manuscript Author Manuscript Author Manuscript Author amplitudes (Extended Data Fig. 4). SST interneurons send inhibitory input to all other cell types, including fast-spiking PV cells25,28. When we examined spontaneous responses of PV cells, we found no influence of locomotive state in P28 mice; by P56, however, PV responses increased when mice ran (Fig. 2a–b). Similarly, running enhanced visually-evoked PV cell responses at P56, but not at P28 (Fig. 2c–d). This increase at P56 is unlikely to be caused by direct actions of acetylcholine on PV cells, as whole-cell recordings from PV cells in acute cortical slices showed no direct responses to carbachol at either P28 or P56 (Fig. 2e–f). This is consistent with prior studies, which show that the modulation of PV responses is indirect22,24,27. Supporting this view, carbachol induced large GABA-mediated inhibitory currents in PV cells at P28 but not at P56 (Fig. 2g–h). These measures indicate that cholinergic action on SST cells and VIP cells drive a strong inhibition of PV cells at P28, but by P56, this inhibition is lessened – a developmental shift opposite to what we found in SST cells. Given these reciprocal differences of the most prominent sources of inhibition to pyramidal neurons, an intriguing question is whether arousal state differently impacts visually-evoked dendritic and somatic responses in critical period versus adult mice. In adult cortex, branch- specific dendritic activity arises during active learning and decision making, and these localized responses facilitate compartmentalized synaptic plasticity4,5. With this in mind, we measured visually-evoked dendritic Ca2+ responses (GCaMP6f) along the apical dendrites of layer 2/3 pyramidal neurons from both age groups. We recorded from sister dendrites,
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